@article {2056, title = {Correlation of Apo E Gene Polymorphism with Recurrent Acute Coronary Syndrome}, journal = {Pharmacognosy Journal}, volume = {15}, year = {2023}, month = {June 2023}, pages = {450-453}, type = {Research Article}, chapter = {450}, abstract = {

Background: Recurrent cardiovascular disease (CVD) incidence puts patients at higher risk for mortality and morbidity. One of the CVD symptoms is acute coronary syndrome (ACS). Many genetic polymorphisms are CVD risk factors. This study{\textquoteright}s purpose was to investigate the correlation between recurrent ACS incidence and apolipoprotein E (ApoE) gene polymorphism. Method: Case-control design was used in this study. About 90 patients who visited the cardiology and internal medicine clinics at UNAIR Hospital in Surabaya, Indonesia, served as the study{\textquoteright}s subjects. There were 30 patients with recurrent ACS, 30 patients with a single ACS, and 30 patients with no history of cardiovascular disease. Afterward, using the polymerase chain reaction-restriction fragment length method, the ApoE gene polymorphism examination was carried out. The Tropical Disease Center UNAIR Laboratory conducted all laboratory testing. Results: In the recurrent ACS group, ApoE polymorphism genotype patterns were 5 subjects for ε2ε2 (16.67\%), 23 subjects for ε3ε3 (76.66\%), and 2 subjects for ε4ε4 (6.67\%). Meanwhile, in the single ACS group, ApoE polymorphism genotype patterns were 6 subjects for ε2ε2 (20\%), 22 subjects for ε3ε3 (73.4\%), 1 subject for ε4ε4 (3.33\%), and 1 subject for ε2ε3 (3.33\%). And, in the non- ACS group, ApoE polymorphism genotype patterns were4 subjects for ε2ε2 (13.34\%), 25 subjects for ε3ε3 (83.33\%), and1 subject for ε4ε4 (3.33\%). There was no correlation of ApoE gene polymorphism with recurrent ACS incidence by Chi-square analysis (p \> 0.05). Conclusion: ApoE gene polymorphism cannot significantly affect recurrent ACS incidence.

}, keywords = {Acute Coronary Syndrome, ApoE gene, PCR RFLP, Polymorphism, Public Health}, doi = {10.5530/pj.2023.15.100}, author = {Muhamad Robiul Fuadi and Jusak Nugraha and I Gde Rurus Suryawan and Hartono Kahar and Aryati and Gwenny Ichsan Prabowo and Budi Utomo and Reny I{\textquoteright}tishom} } @article {1128, title = {Hypoxic Preconditioning Decrease ROS and Increase SOD Expression in Adipose-Derived Mesenchymal Cell}, journal = {Pharmacognosy Journal}, volume = {12}, year = {2020}, month = {May 2020}, pages = {430-435}, type = {Original Article}, chapter = {430}, abstract = {

Adipose-derived Mesenchymal Stem Cells (AMSCs) have promising ability to differentiate into a cardiomyocyte. However, post-transplantation survival of AMSCs is relatively low due to lethal cellular hypoxia. Hypoxic preconditioning is a sublethal hypoxia condition which may improve AMSCs survival. This research evaluates the effect of hypoxic preconditioning on the expression of reactive oxygen species (ROS) and superoxide dismutase (SOD) of AMSCs. Isolated human AMSCs was cultured to the 4th passage and confirmed with CD45, CD90 and CD105 expression. Cells were divided into control group (normoxia with 21\% O2) and hypoxic preconditioning group (with 1\% O2). ROS and SOD were evaluated using immunofluorescence and analyzed using SPSS 25. AMSCs was characterized by the CD105 and CD90 without expression of CD44 and CD45. ROS expression is significantly lower in hypoxia group than in controlled group (253,13 {\textpm} 67,795 vs 342,13 {\textpm} 116,447; p \< 0.05) and SOD expression is significantly higher in hypoxia group than in controlled group (340,25 {\textpm} 96,476 vs 234,56 {\textpm} 38,238; p \<0.05). In conclusion, hypoxic preconditioning in human AMSCs induce lower expression of intracellular ROS and higher expression of intracellular SOD.

}, keywords = {Antioxidant, Hypoxia, Oxidative stress, Stem Cells}, doi = {10.5530/pj.2020.12.66}, author = {I Gde Rurus Suryawan and Andrianto and Ratna Dewi Cahyaningtias and Makhyan Jibril Al-Farabi} }